Ameliorative effects of gallic acid,quercetin and limonene on urethane-induced genotoxicity and oxidative stress in Drosophila melanogaster

The main objective of our present work was to ascertain the efficacy of Drosophila melanogaster model for assessing antigenotoxic and antioxidant effects of dietary phytochemicals gallic acid (GA), quercetin (QC) and limonene (Lim) against urethane (URE), a genotoxic environmental carcinogen. Oregon-K (ORK) adult male flies were fed GA, QC and Lim in combination with URE (20?mM) in 10% sucrose for 72?h. Third instar larvae were fed instant medium containing the above phytochemicals and URE for 24?h. Sex-linked recessive lethal (SLRL) test and assays for estimating glutathione content (GSH), glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD) and lipid peroxidation (MDA content) were performed. Adult feeding experiments demonstrated that co-treatment of flies with URE and the test phytochemicals has significantly decreased the frequencies of SLRL mutations in all the germ cell stages when compared to that with URE alone. Larval feeding experiments also showed a similar pattern. The above results correlate well with antioxidative potentials of the test agents where we observed the elevated enzymatic levels with a significant reduction in MDA level in Drosophila larvae. The results further suggest that the dietary phytochemicals have an antioxidant and antimutagenic property which can be assessed using D. melanogaster.     

Toxicity and teratogenicity of inhaled anesthetics in Drosophila melanogaster

The toxic and teratogenic effects of inhaled anesthetics were assessed in an in vivo assay using the fruit fly Drosophila melanogaster. Eggs were exposed during development (metamorphosis) to enflurane, isoflurane or halothane at a vapor concentration of 0.1 or 0.2% (v/v), to fluroxene at 0.025 or 0.05% (v/v), or to nitrous oxide at 20 or 40% (v/v). Flies produced in each group were counted and were examined for morphological abnormalities within one day of hatching. All the anesthetics except nitrous oxide produced a dose-dependent increase in the duration of metamorphosis and a decrease in the number of flies. Despite these effects on development, no morphological abnormalities were observed in any fly.     

Rotenone mediated developmental toxicity in Drosophila melanogaster

Rotenone (ROT) is a widely used natural pesticide, and its effect on growth and developmental toxicity remain unclear. In the present study, the effects of ROT exposure on the reproductive structure and function of the female Drosophila melanogaster and third instar larvae were investigated. ROT exposure on female Drosophila melanogaster resulted in developmental inhibition and ovarian abnormality, which were evident from the disruptive growth of border cells as well as morphological changes in the orientation of nurse cells during the 9th-10th stage of developing egg chamber of in the Drosophila ovary. Other abnormalities, such as, altered developmental gene expression (Osk, Grk, Nos, Bic-d), inhibition in the kinesin motor protein level (KIF-5B), increased caspases activities (Caspase 3, 8, & 9) and apoptosis were also observed. Subsequently, ROT treated larvae exhibited behavioral deficits and delay in developmental time. The above findings demonstrate that the exposure of ROT causes developmental toxicity in Drosophila melanogaster.     

Coffee mitigates cyclophosphamide-induced genotoxic damage in Drosophila melanogaster germ cells

In the present study, coffee (CF) was evaluated for its protective effects against genotoxic damage and oxidative stress induced by the chemotherapeutic drug, cyclophosphamide (CPH). The sex-linked recessive lethal (SLRL) test was employed to study the induction of mutations in the larvae as well as in all the successive germ cell stages of treated males. Control and treated third instar larvae were used to monitor the biomarkers of oxidative stress response such as glutathione content (GSH), glutathione-S-transferase (GST), catalase (CAT), superoxide dismutase (SOD) and lipid peroxidation (MDA content). Our results demonstrated that co-administration of CF (2%) with CPH (3?mM) has significantly reduced CPH-induced lethal mutations in the germ cells of larvae and adult flies. The reductions observed in mutation frequencies were: 75% in larvae and 62.4% in the adult. Significant enhancement in antioxidant enzymatic levels: CAT (46.6%)?>?SOD (43.0%)?>?GST (42.4%)?>?GSH (31.6%) and reduction in MDA levels (32.05%) in the pretreated third instar larvae demonstrated the antioxidant activity of CF against CPH-induced oxidative stress. The findings from the present study suggest that the Drosophila model is an ideal one for evaluating the antigenotoxic and antioxidant activity of complex mixtures like CF.     

The beneficial effects on blood pressure,dyslipidemia and oxidative stress of Sambucus nigra extract associated with renin inhibitors

Context: The health effects of Sambucus nigra L. (Caprifoliaceae) could be due to polyphenols whose modes of action differ from the traditional one proposed for exogenous antioxidants.

Objective: The study emphasizes the effects of the association between the renin inhibitor and the polyphenolic extract on biochemical parameters and systolic (TAS) and diastolic (TAD) blood pressure within an L NAME-induced experimental model of arterial hypertension (AHT).

Materials and methods: The polyphenols are extracted with ethanol from isolated and purified vegetable material represented by the mature fruit of the S. nigra with a dosage of 0.046?g/kg body weight (PS), every 2 days, for 8 weeks. The dose represents 1/20 of LD₅₀. The Wistar white rat blood pressure values were recorded using a CODA? system, which uses a non-invasive blood pressure measuring method.

Results and discussion: The total antioxidant capacity levels were significantly decreased (p?<?0.001) in AHT group as compared to the rats in the AHT?+?PS group. A combination of a renin inhibitor (Aliskiren) and polyphenolic extract generated a superior antioxidant effect compared to administering the two separately. Both TAS and TAD in rats with drug-induced hypertension were reduced by polyphenolic extract. The homogeneous values of TAS record a significant decrease (p?<?0.001) of the average values in AHT?+?PS group or AHT?+?Aliskiren group.

Conclusion: The combination of two different classes of substances, namely, renin inhibitors and natural polyphenol extracts, reduces arterial pressure and also might reduce the side effects of the major classes of antihypertensive agents and improve the quality of live.     

抗氧化剂茶多酚对哮喘大鼠气道炎症、气道重塑的干预研究

摘要 目的: 研究茶多酚（TP）对支气管哮喘大鼠早期和晚期气道氧化应激水平及气道炎症、气道重塑的影响。 方法: 以卵蛋白为致敏原,通过反复激发,制备大鼠慢性哮喘模型。将48只大鼠随机分为6组：对照组、哮喘组、早期布地奈德（BUD）组、晚期BUD组、早期TP组、晚期TP组。早BUD组、早TP组在造模前2周药物干预,晚BUD组、晚TP组在造模5周后药物干预。造模12周时观察指标①肺组织病理：测定支气管壁的平滑肌面积、胶原沉积面积,以及肺组织转化生长因子-?1（TGF-?1）的表达。②肺组织TGF-β1含量、丙二醛（MDA）含量及超氧化物歧化酶（SOD）活力。 结果: ①早TP组、晚TP组、早BUD组干预后各项气道重塑指标较哮喘组均有改善（P＜0.01或P＜0.05),早TP组改善最明显(P均＜0.01)。晚BUD组较哮喘组无明显改善(P＞0.05)。②哮喘组肺组织中MDA含量明显上升,SOD活性显著下降,与对照组有显著性差异(P＜0.01);各药物干预后SOD活性均上升,MDA含量均下降,以早TP组最明显(P＜0.01)。③相关性分析表明,SOD活性与MDA含量呈负相关,支气管壁的胶原沉积面积与MDA含量呈正相关。 结论: 茶多酚可能通过清除氧自由基,减少气道炎症及氧化应激,从而改善或延缓气道重塑的发生。     

Effect of alloxan on the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ)Bg9

Abstract

The third instar larvae were allowed to feed on the diet having 0.001–0.004?M of alloxan in the diet for 24?h. The larvae were collected and were analyzed for hsp70 expression and tissue damage. The larvae homogenate was used for estimating GSH content, GST activity, LPO, PCC, and glucose content. The activity of caspase 3 and 9, apoptotic index, and DNA damage was estimated in the midgut cells of the larvae exposed to various doses of alloxan. The results suggest that alloxan is toxic at 0.002, 0.003, and 0.004?M without alteration in glucose content.     

Mutagenic effects of fluphenazine hydrochloride in Drosophila melanogaster

The mutagenic potential of fluphenazine hydrochloride was tested on male germ cells of Drosophila melanogaster. The criterion used was sex-linked recessive lethal mutations. Oregon-K males of D. melanogaster, reared on a medium containing 0.01, 0.02 and 0.03 mg/ml of the drug, were screened for sex-linked recessive lethal mutations. The incidence of sex-linked lethals was significant. The results clearly demonstrate that fluphenazine is capable of inducing recessive lethal mutations in Drosophila especially in pre-meiotic stages of spermatogenesis.     

The protective effects of astaxanthin against cisplatin-induced retinal toxicity

Purpose: This study investigated the toxic effects of an antineoplastic agent, cisplatin (CIS), on retinal cells and the potential capacity of astaxanthin (ASTA) to elicit a future therapeutic protocol in CIS-induced retinal toxicity.

Materials and methods: Six groups were formed for the assessment; control (healthy; Group 1), olive oil (olive oil only; Group 2), ASTA control group (ASTA only, Group 3), the single intraperitoneal (IP) dose of 16?mg/kg CIS (CIS only group; Group 4), 16?mg/kg CIS +25?mg/kg (IP) ASTA (Group 5), and 16?mg/kg CIS +75?mg/kg (IP) ASTA (Group 6). On the third day after CIS administration, rats in all groups were sacrificed under anesthesia and the analysis of the biochemical parameters and histopathological levels were performed.

Results: A significant decrease in GSH levels and increases in MDA, eNOS, and 8-OHdG expressions were recorded. Additionally, CIS treatment had caused acidophilic staining in retinal histological appearance. ASTA treatment reduced the increases in MDA, eNOS, and 8-OHdG levels following CIS administration and increased the levels of GSH expressions, as well.

Conclusions: These results may suggest that the ASTA molecule as a promising option to prevent retinal toxicity in patients receiving CIS treatment for malignant tumors.     

Paracetamol: overdose-induced oxidative stress toxicity,metabolism, and protective effects of various compounds in vivo and in vitro

Paracetamol (APAP) is one of the most widely used and popular over-the-counter analgesic and antipyretic drugs in the world when used at therapeutic doses. APAP overdose can cause severe liver injury, liver necrosis and kidney damage in human beings and animals. Many studies indicate that oxidative stress is involved in the various toxicities associated with APAP, and various antioxidants were evaluated to investigate their protective roles against APAP-induced liver and kidney toxicities. To date, almost no review has addressed the APAP toxicity in relation to oxidative stress. This review updates the research conducted over the past decades into the production of reactive oxygen species (ROS), reactive nitrogen species (RNS), and oxidative stress as a result of APAP treatments, and ultimately their correlation with the toxicity and metabolism of APAP. The metabolism of APAP involves various CYP450 enzymes, through which oxidative stress might occur, and such metabolic factors are reviewed within. The therapeutics of a variety of compounds against APAP-induced organ damage based on their anti-oxidative effects is also discussed, in order to further understand the role of oxidative stress in APAP-induced toxicity. This review will throw new light on the critical roles of oxidative stress in APAP-induced toxicity, as well as on the contradictions and blind spots that still exist in the understanding of APAP toxicity, the cellular effects in terms of organ injury and cell signaling pathways, and finally strategies to help remedy such against oxidative damage.     

Effect of quercetin on lipopolysaccharide induced-sickness behavior and oxidative stress in rats

Objectives:

Gram-negative infections and control infusion of recombinant cytokines in human have been shown to induce sickness behavior characterized by fever, prolong sleep, decreased food and water intake, reduced mobility, depression, and anxiety. Therefore, the present study was undertaken to investigate the effect of bioflavonoid quercetin in lipopolysaccharide (LPS)-induced sickness behavior.

Materials and Methods:

Wistar albino rats were divided into six groups (n=6). Three groups received vehicle and two doses of quercetin (2 and 25 mg/kg, i.p.) respectively for 2 weeks before being challenged with LPS (1 mg/kg, i.p). One group received vehicle for 2 weeks and was challenged with saline on day 15. The per se effect of quercetin (2 and 25 mg/kg, i.p.) was also seen after 2 weeks of dosing. LPS-induced sickness behavior in rats was quantified by measuring time in social exploration, anxiety, food and water consumption, and weight loss. Levels of cytokines (TNF-α, IL-1β, and IL-6) and oxidative stress in rat brain were also analyzed.

Results:

Quercetin (2 and 25 mg/kg) administration significantly (P<0.05) attenuated LPS-induced sickness behavior by modulating cytokines production as well inhibiting LPS-induced oxidative stress.

Conclusions:

Adequate intake of dietary flavonoids (like quercetin) may help promote recovery from sickness behavior.     

Urtica dioica attenuates ovalbumin-induced inflammation and lipid peroxidation of lung tissues in rat asthma model

Context: To find bioactive medicinal herbs exerting anti-asthmatic activity, we investigated the effect of an aqueous extract of Urtica dioica L. (Urticaceae) leaves (UD), the closest extract to the Algerian traditional use.

Objective: In this study, we investigated the in vivo anti-asthmatic and antioxidant activities of nettle extract.

Materials and methods: Adult male Wistar rats were divided into four groups: Group I: negative control; group II: Ovalbumin sensitized/challenged rats (positive control); group III: received UD extract (1.5?g/kg/day) orally along the experimental protocol; group IV: received UD extract (1.5?g/kg/day) orally along the experimental protocol and sensitized/challenged with ovalbumin. After 25?days, blood and tissue samples were collected for haematological and histopathological analysis, respectively. The oxidative stress parameters were evaluated in the lungs, liver and erythrocytes. Then, correlations between markers of airway inflammation and markers of oxidative stress were explored.

Results: UD extract significantly (p?p?50 value.

Conclusions: The results confirmed that UD administration might be responsible for the protective effects of this extract against airway inflammation.     

The toxicological effects of nano titanium dioxide on target organs and mechanisms of toxicity

Nano-titanium dioxide (TiO₂NPs) is widely used for its extremely high stability, corrosion resistance, and photocatalytic properties and has penetrated into various fields of production and life. Assessing its toxicity to different organs should be a key part of preclinical toxicity assessment of TiO₂NPs, which is relatively incomprehensive yet. Therefore, this review focuses on the toxic effects of TiO₂NPs on various organs in mammals and biological mechanisms from different organs. The commonality of toxic effects on various target organs reflected in tissue structure damage and dysfunction, such as liver damage and dysfunction; pulmonary fibrosis; and renal impairment (including hematuria and nephritis); damage of brain tissue and neurons; alteration of intestinal villi; and weight loss. And effects on the reproductive system are affected by different sexes, including ovarian dysfunction, testicular development damage, and sperm viability reduction. We believe that the toxic mechanisms of TiO₂NPs in target organs have commonalities, such as oxidative stress, inflammatory responses, and organelle damage. However, different target organ toxicities also have their specificities. TiO₂NPs disturb the intestinal flora and cause undesirable changes in feces products. And in spleen are infiltration of neutrophils and lymphadenopathy and eventually immune deficiency. Although the toxic pathways are different, but there may be a close link between the different toxic pathways. In this article, the main manifestations of the toxic effects of titanium dioxide nanoparticles on major mammalian organs are reviewed, in order to provide basic data for their better application from a medical perspective.     

Hydroxytyrosol,a dietary phenolic compound forestalls the toxic effects of methylmercury‐induced toxicity in IMR‐32 human neuroblastoma cells

This study demonstrates the protective potential of hydroxytyrosol (HT), an olive oil phenol, against methylmercury (MeHg)‐induced neurotoxicity using IMR‐32 human neuroblastoma cell line. HT inhibited MeHg‐induced cytotoxicity and genotoxicity as confirmed by MTT, micronucleus, and comet assays. Cells preconditioned with HT showed reduction of MeHg‐induced cellular oxidative stress along with the maintenance of glutathione, superoxide dismutase, glutathione‐S‐tranferase, and catalase. Fluorescence microscopy and DNA ladder assays indicated the inhibitory effect of HT against MeHg‐induced apoptosis, which was further established by Western blotting. An effective concentration of 5 µM HT caused downregulation of p53, bax, cytochrome c, and caspase 3 and upregulation of prosurvival proteins including nuclear factor erythroid 2‐related factor 2 (Nrf2) and metallothionein. This work indicates the cytoprotective potential of HT against MeHg‐induced toxicity primarily by the lowering of oxidative stress, which may be endorsed to its antigenotoxic and antiapoptotic potential, in addition to its free radical scavenging ability. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1264–1275, 2016.     

The mutagenic and toxic effects of bleomycin and trifluoperazine in Drosophila melanogaster

The mutagenic and toxic effects of trifluoperazine and bleomycin on Drosophila were investigated in the progenies of males injected with 0.2 microliter of bleomycin and/or trifluoperazine. The Muller-5 method was used to study the induction of complete- and mosaic-sex-linked recessive lethals induced by 0.1 microgram/ml bleomycin and/or 0.1 mM trifluoperazine in the five successive broods, mainly representing the different stages of spermatogenesis. Trifluoperazine increased the induction rate of sex-linked recessive mutations above the spontaneous rates of the control, but these increases were not statistically significant at the 5% level27 in any of the five different broods. Contrary to trifluoperazine, bleomycin significantly (5% level)27 increased the induction rate of the complete sex-linked recessive lethals over those of the control in the meiotic and premeiotic broods C and D, and the meiotic brood E. As with the separate treatment with bleomycin, the frequencies of the complete sex-linked recessive lethals induced by the simultaneous combination treatment of 0.1 microgram/ml bleomycin and 0.1 mM trifluoperazine were significantly higher than those of the control at the 5%27 level, only in the meiotic and premeiotic broods, but they were not significantly higher than those induced by bleomycin treatment alone19. Treatments with 0.1 mM trifluoperazine enhanced the toxicity, sterility and the number of mutated clusters induced by 0.1 mM bleomycin but did not significantly increase the rates of induced lethals over the additive effects of both drugs in the meiotic and premeiotic stages, suggesting no potentiation effects for trifluoperazine over those of bleomycin in Drosophila. Higher concentrations of the two drugs could not be used due to their high toxicity and sterility effects.     

Protective effects of Ziziphora tenuior extract against chlorpyrifos induced liver and lung toxicity in rat: Mechanistic approaches in subchronic study

Chlorpyrifos (CPF) is one of the most widely used organophosphorus, which has spurred renewed interest. This study was conducted to investigate the protective effect of ziziphora tenuior extract against CPF‐induced liver and lung toxicity. This study conducted 8‐week rat sub‐chronic toxicity study and then the effect of ziziphora tenuior extract in 3 different doses (40, 80, 160 mg/kg) was determined. We administrated maximum tolerated dose of CPF (6.75 mg/kg) by gavage for 8 weeks (5 times in week) to male rats. Rats were sacrificed 24 h after last dose and the biochemical analysis, which confirms involvement of oxidative stress in the pathogenesis of CPF toxicity in liver including increased in lipid peroxidation, protein carbonyl content, and ROS formation, glutathione depletion, decreased of antioxidant effect via frap oxidation and cytochrome c expulsion. In addition, pathological lesions confirm the dysfunction of the organs (liver and lung). In addition, using of ziziphora extract as an antioxidant is resulted in amelioration of oxidative stress marker in liver and lung damage. In conclusion, the current study revealed that CPF toxicity is related to oxidative stress and induction of cell death signaling and cotreatment with ziziphora extract is recommended in the routine therapy for the protection against CPF induced liver and lung tissue damage.     

Protection by apple peel polyphenols against indometacin‐induced oxidative stress,mitochondrial damage and cytotoxicity in Caco‐2 cells

Objectives Exposure of Caco‐2 cells to indometacin can be a useful model to assess some of the cytotoxic events that appear to underlie the gastrointestinal lesions associated with the use of this anti‐inflammatory agent. Using such a cellular model, we addressed here the cytoprotective potential of a recently standardized apple peel polyphenol extract, APPE. Methods We firstly characterized APPE in terms of its free radical scavenging and antioxidant properties, and subsequently investigated its potential to protect Caco‐2 cells against the deleterious effects of indometacin on cellular oxidative status (redox state, malondialdehyde, glutathione (GSH) and oxidized glutathione (GSSG) levels), mitochondrial function (ATP and mitochondrial membrane potential) and cell viability (3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) reduction and lactate dehydrogenase (LDH) leakage). For comparative purposes, the free radical scavenging properties and reducing capacity of quercetin, epicatechin and rutin were also estimated. Key findings In the absence of APPE, indometacin induced mitochondrial perturbations (reducing ATP and the mitochondrial membrane potential), enhanced the oxidative status (decreasing the GSH/GSSG ratio and increasing dichlorofluorescein oxidation and malondialdehyde) and lowered the cell viability (decreasing MTT reduction and increasing LDH leakage). APPE, whether pre‐added or co‐incubated with indometacin, concentration‐dependently prevented these mitochondrial, oxidative and cell viability alterations. Prompted by the recently recognized ability of indometacin to enhance the mitochondrial formation of reactive oxygen species, APPE was also characterized in terms of its free radical‐scavenging capacity. APPE was found to actively scavenge O₂·^‐, HO· and peroxyl radicals. Such free radical‐scavenging activity of APPE suggests that its ability to protect mitochondria and prevent the oxidative and lytic damage induced by indometacin arises from its potent antioxidant capacity. Conclusions In Caco‐2 cells APPE prevented mitochondrial oxidative and cell viability alterations induced by indometacin possibly through its ability to scavenge reactive oxygen species. These findings are of interest in view of the high prevalence of gastrointestinal side‐effects associated with the use of conventional anti‐inflammatory agents.     

Anti-angiogenic effects of two cystine-knot miniproteins from tomato fruit

BACKGROUND AND PURPOSE

Cystine-knot miniproteins are characterized by a similar molecular structure. Some cystine-knot miniproteins display therapeutically useful biological activities, as antithrombotic agents or tumour growth inhibitors. A critical event in the progression of tumours is the formation of new blood vessels. The aim of this work was to test two tomato cystine-knot miniproteins for their effects on endothelial cell proliferation and angiogenesis in vitro.

EXPERIMENTAL APPROACH

Two tomato cystine-knot miniproteins (TCMPs) were expressed and purified either as recombinant or as native proteins from tomato fruits. The Matrigel assay was used to investigate the effects of TCMPs on in vitro angiogenesis. Viability and proliferation of endothelial cells were tested. Extracellular signal-regulated kinase (ERK)1/2 phosphorylation was assayed in either HUVEC or A431 epidermal growth factor receptor (EGFR)-overexpressing cells treated with TCMPs. EGFR phosphorylation was tested in A431 cells.

KEY RESULTS

Both recombinant and native TCMPs inhibited in vitro angiogenesis of HUVEC cells at concentrations of 15–100 nM. The anti-angiogenic effect of TCMPs was associated with the inhibition of ERK phosphorylation. The two miniproteins did not alter the viability and proliferation of the endothelial cells.

CONCLUSIONS AND IMPLICATIONS

The anti-angiogenetic properties of TCMPs are of potential pharmacological interest because they are common and natural components of the human diet, they possess low toxicity, they are active at submicromolar concentrations, they share a common molecular structure that can be used as a molecular platform for the design of molecules with enhanced biological activity.     

Mutagenic effects of gold nanoparticles induce aberrant phenotypes in Drosophila melanogaster

The peculiar physical/chemical characteristics of engineered nanomaterials have led to a rapid increase of nanotechnology-based applications in many fields. However, before exploiting their huge and wide potential, it is necessary to assess their effects upon interaction with living systems. In this context, the screening of nanomaterials to evaluate their possible toxicity and understand the underlying mechanisms currently represents a crucial opportunity to prevent severe harmful effects in the next future. In this work we show the in vivo toxicity of gold nanoparticles (Au NPs) in Drosophila melanogaster, highlighting significant genotoxic effects and, thus, revealing an unsettling aspect of the long-term outcome of the exposure to this nanomaterial. After the treatment with Au NPs, we observed dramatic phenotypic modifications in the subsequent generations of Drosophila, demonstrating their capability to induce mutagenic effects that may be transmitted to the descendants. Noteworthy, we were able to obtain the first nanomaterial-mutated organism, named NM-mut. Although these results sound alarming, they underline the importance of systematic and reliable toxicology characterizations of nanomaterials and the necessity of significant efforts by the nanoscience community in designing and testing suitable nanoscale surface engineering/coating to develop biocompatible nanomaterials with no hazardous effects for human health and environment. FROM THE CLINICAL EDITOR: While the clinical application of nanomedicine is still in its infancy, the rapid evolution of this field will undoubtedly result in a growing number of clinical trials and eventually in human applications. The interactions of nanoparticles with living organisms determine their toxicity and long-term safety, which must be properly understood prior to large-scale applications are considered. The paper by Dr. Pompa's team is the first ever demonstration of mutagenesis resulting in clearly observable phenotypic alterations and the generation of nano-mutants as a result of exposure to citrate-surfaced gold nanoparticles in drosophila. These groundbreaking results are alarming, but represent a true milestone in nanomedicine and serve as a a reminder and warning about the critical importance of "safety first" in biomedical science.     

The effect of aqueous extract of Rosa damascena on formaldehyde-induced toxicity in mice testes

Context: Rosa damascena L. (Rosaceae) (RD) essential oil and extracts are commonly used as a flavour in herbal medicine which increase libido. Previous studies have shown inhalation of RD flower’s oil increases libido and causes protective effects in formaldehyde (FA)-induced testicular damage.

Objective: The protective effects of aqueous extract of RD on the male reproductive system of mice were examined following FA-induced damage.

Materials and methods: Forty-eight adult NMRI male mice were randomly assigned to six groups (n?=?8): control (normal saline, 10?mg/kg); RD40 (40?mg/kg, p.o.); FA treated (10?mg/kg of 10%, i.p.) and FA?+?RD treated at 10, 20 and 40?mg/kg (FA?+?RD10), (FA?+?RD20) and (FA?+?RD40), respectively, for 40 days. At the end of treatment regimes, serum testosterone (T) level and the reproductive activity, viz. body/organ weights, testicular structure and sperm characteristics were studied.

Results: Formaldehyde administration significantly decreased serum T level (p?p?p?Discussion and conclusions: We may conclude that RD flower extract can withstand effects of FA in the male reproductive system of mice possibly due to its antioxidative properties.